Re : Articles importants dans Nature, Science ou Cell
Il s'agit de la dynéine, voir infos et commentaire sur le Bactérioblog (blog scientifique).Envoyé par Gaïalhambra
Vraiment c'est magnifique...
Merci beaucoup pour ce lien !
Il y a pourtant une ou deux choses que je n'ai pas reconnues, notament la grosse prot qui se déplace comme en marchant ?!
Pas vraiment un article scientifique, mais pour mon tout premier message j'ai trouvé sympa de mettre ce lien vers Nature (en plus il est gratuit!).
Histoire de rassurer tous les thésards neurasténiques...
http://www.nature.com/naturejobs/200...#related-links
... et d'aider ceux qui n'ont pas encore fait leur choix à devenir chercheur en toute connaissance de cause !
Très bon article
J'ai enfin réussi à mettre des mots sur ce que je pense depuis longtemps....
A+
Vinc
Salut,
Bon je propose une très courte revue de Cell (ou plutot un editorial), qui n'est malheureusement pas en libre accès (code biblioinserm ou bibliovie requis).
On voit qu'il n'y a pas qu'en France que la recherche publique coule, même aux US ils s'y mettent... : A lost generation.
A+.
Voilà une publie de JMB (Journal of Molecular Biology) qui présente une nouvelle méthode de prédiction de structure protéique par ordinateurs :
Computational protein design.
Donc elle pourrait être une méthode remplaçant peu à peu notre bonne vieille cristallo, mais en y réfléchissant bien ça pourrait être génial pour prédire la structure des protéines membranaires qui sont presque 'incristallisables".
Dans ce papier, ils mettent en avant la structure de protéines déterminées par cristallo et RMN, donc du concret, et ils les comparent avec les structures trouvées par ordinateur grace à un programme nommé Rosetta. Les superpositions sont stupéfiantes, quasiment parfaites!
Il faut tout de même noter que ce programme Rosetta est lié à la plateforme de calcul partagé Boinc. Cette publi fait référence au pré-Boinc pour ce projet, dont le directeur de recherche David Baker a fait appel vu la puissance de calcul requise pour déterminer les structures de protéines par ordinateurs. Il y a d'ailleurs 2 publis qui vont sortir prochainement (dans un ou deux mois) sur 8 protéines déterminées grace à Boinc et les utilisateurs qui les ont trouvées vont apparaitre dans ces publis (il y en a 28 au total). Donc Boinc c'est pas du superflu...........loin de là!
A+
Bonsoir
UN article tres surprenant! des chercheurs ont réussit a rendre lineaire le génome de E. coli! (alors que celui-ci est normalement circulaire).
Le plus surprenant est qu'il ne semble pas y avoir de gros defaut...
http://www.nature.com/embor/journal/...s/7400880.html
YOyo
Salut!
Dans la série "on croyait avoir comprit mais en fait on a tout faux", voici la mutation silencieuse qui modifit les propriétés de la protéine!
A “Silent” Polymorphism in the MDR1 Gene Changes Substrate Specificity.
Chava Kimchi-Sarfaty, Jung Mi Oh, In-Wha Kim, Zuben E. Sauna,
Anna Maria Calcagno, Suresh V. Ambudkar, Michael M. Gottesman
Synonymous single-nucleotide polymorphisms (SNPs) do not produce altered coding sequences, and therefore they are not expected to change the function of the protein in which they occur.
We report that a synonymous SNP in the Multidrug Resistance 1 (MDR1) gene, part of a haplotype previously linked to altered function of the MDR1 gene product P-glycoprotein (P-gp), nonetheless results in P-gp with altered drug and inhibitor interactions. Similar mRNA and protein levels, but altered conformations, were found for wild-type and polymorphic P-gp. We hypothesize that the presence of a rare codon, marked by the synonymous polymorphism, affects the timing of cotranslational folding and insertion of P-gp into the membrane, thereby altering the structure of substrate and inhibitor interaction sites.
www.sciencemag.org SCIENCE VOL 315 26 JANUARY 2007
http://www.ncbi.nlm.nih.gov/entrez/q...=pubmed_docsum
A+
Vinc
merci vinc on te voit peu mais c'est efficace quand tu passes
L'article a l'air d'etre genial!
Yoyo
Oui et comme je suis un seigneur j'en rajoute une couche avec cette fois ci un très beau papier. En gros ils ont regardé le kinome (soit environ 500 kinases) humain dans plus de 200 cancers..... Pour infos, les "supplementary data and tables" font 130 pages......
Je vous passe la liste d'auteurs car ils sont assez nombreux
Patterns of somatic mutation in human cancer genomes.
Cancers arise owing to mutations in a subset of genes that confer growth advantage. The availability of the human genome sequence led us to propose that systematic resequencing of cancer genomes for mutations would lead to the discovery of many additional cancer genes. Here we report more than 1,000 somatic mutations found in 274 megabases (Mb) of DNA
corresponding to the coding exons of 518 protein kinase genes in 210 diverse human cancers. There was substantial variation in the number and pattern of mutations in individual cancers reflecting different exposures, DNA repair defects and cellular origins. Most somatic mutations are likely to be ‘passengers’ that do not contribute to oncogenesis. However, there was
evidence for ‘driver’ mutations contributing to the development of the cancers studied in approximately 120 genes. Systematic sequencing of cancer genomes therefore reveals the evolutionary diversity of cancers and implicates a larger repertoire of cancer genes than previously anticipated.
Si vous n'avez pas la possibilité d'avoir le PDF et que vous voulez avoir accés aux data = MP.
A+
Vinc
Salut,
Voici un papier très récent qui est sorti sur l'étude de la méthylation de 16000 promoteurs humains, sur lignés somatique et germinale. Vous verrez qu'il y a des "paradoxes" entre le taux de méthylation de certains gènes et leur activité, et que la méthylation de l'histone H3 jouerait un rôle important dans la protection de certains promoteurs de la méthylation, ce qui expliquerait la non-méthylation de gènes inactifs.
L'abstract : Distribution, silencing potential and evolutionary impact of promoter DNA methylation in the human genome
modification du lien! Yoyo
A+
Bonjour,
Voici une nouvelle technique assez révolutionnaire. Malgré le fait qu'elle soit toute nouvelle et donc qu'elle n'a pas pu être éprouvée, je pense réellement qu'elle a le potentiel d'améliorer efficacement la génération de souris KO, surtout au niveau de l'économie de temps et d'argent. C'est un Nature Biotechnology.
Le lien vers l'abstract : F0 generation mice
Et voici l'abstract :
A useful approach for exploring gene function involves generating mutant mice from genetically modified embryonic stem (ES) cells. Recent advances in genetic engineering of ES cells have shifted the bottleneck in this process to the generation of mice. Conventional injections of ES cells into blastocyst hosts produce F0 generation chimeras that are only partially derived from ES cells, requiring additional breeding to obtain mutant mice that can be phenotyped. The tetraploid complementation approach directly yields mice that are almost entirely derived from ES cells, but it is inefficient, works only with certain hybrid ES cell lines and suffers from nonspecific lethality and abnormalities, complicating phenotypic analyses. Here we show that laser-assisted injection of either inbred or hybrid ES cells into eight cell-stage embryos efficiently yields F0 generation mice that are fully ES cell-derived and healthy, exhibit 100% germline transmission and allow immediate phenotypic analysis, greatly accelerating gene function assignment.
Greg
Bonjour,
Je vous propose ma contribution à ce thread de veille scientifique
Cette semaine dans Nature un bel exemple de ce qu'on peut faire avec les crédits démentiels de gros labos americain.
De la "force brute" génétique :
"Genome-wide association study of 14,000 cases of seven common diseases and 3,000 shared controls"
avec tout plein d'auteurs dedans bien sûr.
Mais la vrai star du papier, c'est la méthode d'association génétique entre des marqueurs polymorphes (SNP) et des gènes impliqués dans diverses pathologies humaines.
Le principe, c'est d'utiliser une puce qui révèle les haplotypes de - tenez vous - environ 500,000 locus par individu testé ( pour une cohorte de 14000 "malades" et 3000 "contrôles" ca en fait des data
Des statistiques donc, basées sur le deséquilibre de liaison qu'il peut y avoir chez les "malades" entre un locus neutre et un locus impliqué dans la pathologie (désequilibre qui n'existe pas chez les contrôles).
Une vingtaine de nouveaux gènes impliqués ont été découverts à cette occasion.
Le lien :
article
l'abstract :
There is increasing evidence that genome-wide association (GWA) studies represent a powerful approach to the identification of genes involved in common human diseases. We describe a joint GWA study (using the Affymetrix GeneChip 500K Mapping Array Set) undertaken in the British population, which has examined 2,000 individuals for each of 7 major diseases and a shared set of 3,000 controls. Case-control comparisons identified 24 independent association signals at P < 5 10-7: 1 in bipolar disorder, 1 in coronary artery disease, 9 in Crohn's disease, 3 in rheumatoid arthritis, 7 in type 1 diabetes and 3 in type 2 diabetes. On the basis of prior findings and replication studies thus-far completed, almost all of these signals reflect genuine susceptibility effects. We observed association at many previously identified loci, and found compelling evidence that some loci confer risk for more than one of the diseases studied. Across all diseases, we identified a large number of further signals (including 58 loci with single-point P values between 10-5 and 5 10-7) likely to yield additional susceptibility loci. The importance of appropriately large samples was confirmed by the modest effect sizes observed at most loci identified. This study thus represents a thorough validation of the GWA approach. It has also demonstrated that careful use of a shared control group represents a safe and effective approach to GWA analyses of multiple disease phenotypes; has generated a genome-wide genotype database for future studies of common diseases in the British population; and shown that, provided individuals with non-European ancestry are excluded, the extent of population stratification in the British population is generally modest. Our findings offer new avenues for exploring the pathophysiology of these important disorders. We anticipate that our data, results and software, which will be widely available to other investigators, will provide a powerful resource for human genetics research.
Je ne propose pas d'article, car je dois déjà lire tt ceux présents sur ce post et je n'aurais pas le temps...
Je vous remercie largement pour l'initiative! Génial! Parfait !
Un article qui me parait intéressant:
J Mol Biol. 2007 Jun 22;369(5):1200-13. Epub 2007 Apr 20.Click here to read Links
Modelling transcriptional interference and DNA looping in gene regulation.
Dodd IB, Shearwin KE, Sneppen K.
Centre for Models of Life, Niels Bohr Institute, Blegdamsvej 17, 2100 Copenhagen Ø, Denmark; Molecular and Biomedical Sciences (Biochemistry), University of Adelaide SA 5005, Australia.
We describe a hybrid statistical mechanical and dynamical approach for modelling the formation of closed, open and elongating complexes of RNA polymerase, the interactions of these polymerases to produce transcriptional interference, and the regulation of these processes by a DNA-binding and DNA-looping regulatory protein. As a model system, we have used bacteriophage 186, for which genetic, biochemical and structural studies have suggested that the CI repressor binds as a 14-mer to form alternative DNA-looped complexes, and activates lysogenic transcription indirectly by relieving transcriptional interference caused by the convergent lytic promoter. The modelling showed that the original mechanisms proposed to explain this relief of transcriptional interference are not consistent with the available in vivo reporter data. However, a good fit to the reporter data was given by a revised model that incorporates a novel predicted regulatory mechanism: that RNA polymerase bound at the lysogenic promoter protects itself from transcriptional interference by recruiting CI to the lytic promoter. This mechanism and various estimates of in vivo biochemical parameters for the 186 CI system should be testable. Our results demonstrate the power of mathematical modelling for the extraction of detailed biochemical information from in vivo data.
PMID: 17498740 [PubMed - in process]
Errata
Sont anglais en fait !!! (c'est peut-être pour cela qu'il y a 40 labo dans le coup)Bonjour,
Je vous propose ma contribution à ce thread de veille scientifique
Cette semaine dans Nature un bel exemple de ce qu'on peut faire avec les crédits démentiels de gros labos americains.
Re : Articles importants dans Nature, Science ou Cell
Je me permets de mentionner ici un nouveau blog (pas de moi) qui va s'atteler à des comptes-rendus (critiques) en français des dernières publis en bio-informatique, génétique et biologie moléculaire, parues dans les revues les plus importantes :
Papiers aléatoires
Salut,
Voici un Nature qui a un bon potentiel de "scoop" : Cdk1 est la seule Cdk vraiment essentielle au cycle cellulaire chez les mammifères! Un gros paquet de résultats et des KO dans tous les sens, typique d'un bon Nature!!
Cdk1 is sufficient to drive the mammalian cell cycle
J'avais oublié de dire que les travaux ont été dirigés par Mariano Barbacid, une des références dans l'étude du cycle cellulaire.
A+. Greg.
Moi je l'ai vu en confeeeeeeee!
V.
Bonjour a tous je voudrais proposer un extrait ds nature biotechnology prometteur je pense ,
RNase H-mediated retrovirus destruction in vivo
triggered by oligodeoxynucleotides
Kathrin Matzen1–3, Lina Elzaouk1,3, Alexey A Matskevich1,3, Anja Nitzsche2, Jochen Heinrich1 &
Karin Moelling1
The HIV-1 RNase H can be prematurely activated by
oligodeoxynucleotides targeting the highly conserved polypurine
tract required for second strand DNA synthesis1–5. This inhibits
retroviral replication in cell-free HIV particles and newly
infected cells1–4. Here we extend these studies to an
in vivo model of retroviral replication. Mice that are chronically
infected with the spleen focus-forming virus and treated with
oligodeoxynucleotides that target the polypurine tract, exhibit
either transient or long-term reductions in plasma virus titer,
depending on the therapeutic regimen. Treatment prior to,
during or shortly after infection can delay disease progression,
increase survival rates and prevent viral infection. This strategy
destroys viral RNA template in virus particles in serum as well
as early retroviral replication intermediates in infected cells.
As it targets events common to the replication cycle of all
retroviruses, this approach may be broadly applicable to
retroviruses of medical and agricultural importance.
L.
Petit article sur la découverte de la réponse UPR...
Science 3 December 1999:
Vol. 286. no. 5446, pp. 1888 - 1893
DOI: 10.1126/science.286.5446.1888
Review
Posttranslational Quality Control: Folding, Refolding, and Degrading Proteins
Sue Wickner, 1 Michael R. Maurizi, 2 Susan Gottesman 1*
Polypeptides emerging from the ribosome must fold into stable three-dimensional structures and maintain that structure throughout their functional lifetimes. Maintaining quality control over protein structure and function depends on molecular chaperones and proteases, both of which can recognize hydrophobic regions exposed on unfolded polypeptides. Molecular chaperones promote proper protein folding and prevent aggregation, and energy-dependent proteases eliminate irreversibly damaged proteins. The kinetics of partitioning between chaperones and proteases determines whether a protein will be destroyed before it folds properly. When both quality control options fail, damaged proteins accumulate as aggregates, a process associated with amyloid diseases.
1 Laboratory of Molecular Biology, National Cancer Institute, Bethesda, MD 20892-4255, USA.
2 Laboratory of Cell Biology, National Cancer Institute, Bethesda, MD 20892-4255, USA.
Un article génial et des conséquences immenses avec la découverte de la réponse UPR , les liens avec l'apoptose ("role of the unfolded protein reponse in cell death" 2006, Apoptosis, R.Kim, M. Emi,...) et les liens vers de nombreuses maladies...
Amicalement,
Greg
Bonjour a tous
Alors voila moi chui microbiologiste. Et voila le ti papier que je propose.
Bug juice: Harvesting electricity with microorganisms
Lovley D Nature Reviews Microbiolgy vol 4 July 2006 497-508
tres interesant. Les microbes sont nos amis (enfin qq uns).
Et puis apres quand on postule chez EDF en recherche et dev ya rien! Pfff
Aller a plus les cocos
Bonjour à tous!
Un papier assez vieux que j'aurai dû mettre il y a longtemps...
J Biol Chem. 2004 Oct 1;279(40):41414-21. Epub 2004 Jul 14.
The Tumor Suppressor Protein p16INK4a and the Human Papillomavirus Oncoprotein-58 E7 Are Naturally Occurring Lysine-less Proteins That Are Degraded by the Ubiquitin System.
DIRECT EVIDENCE FOR UBIQUITINATION AT THE N-TERMINAL RESIDUE.
Ronen Ben-Saadon, Ifat Fajerman, Tamar Ziv, Ulf Hellman¶, Alan L. Schwartz||**, and Aaron Ciechanover
Conjugation of ubiquitin to an internal lysine is the initial step in the degradation of the majority of the substrates of the ubiquitin system. For several substrates, it has been shown that the first ubiquitin moiety is conjugated to the N-terminal residue. In all these substrates, however, the internal lysines also played a role in modulating their stability. To better understand the physiological significance of this novel mode of modification, it was important to identify proteins in which degradation is completely dependent on N-terminal ubiquitination. Also, although the experimental evidence for N-terminal ubiquitination is rather strong, nevertheless, it has remained indirect. Here we demonstrate that an important group of proteins that are targeted via N-terminal ubiquitination are the naturally occurring lysine-less proteins such as the human papillomavirus (HPV)-58 E7 oncoprotein and the cell cycle inhibitor and tumor suppressor p16(INK4a). For these proteins, the only residue that can be targeted is the N-terminal residue. Interestingly, p16(INK4a) is degraded in a cell density-dependent manner. Importantly, we provide for the first time direct evidence for N-terminal ubiquitination. Analysis of tryptic digest of the ubiquitin conjugate of HPV-58 E7 revealed a fusion peptide that is composed of the C-terminal domain of ubiquitin and the N-terminal domain of E7. With the abundance of native lysine-less proteins, among which are important viral and cell regulators, this novel mode of protein targeting has implications for both physiological and pathophysiological processes.
L'article est accecible gratuitement, merci JBC....
http://www.jbc.org/cgi/reprint/279/40/41414http://www.jbc.org/cgi/reprint/279/40/41414
Pour la petite histoire, Aaron Ciechanover a reçu le Prix Nobel de chimie en 2004 (avec 2 autres chercheurs) pour la découverte de l'UPS...
V.
Je ne peux pas resister a poster cet article paru dans le dernier numero de Nature (450, p56-62)
(lien)... un bel exemple de l'utilisation des techniques de recombinaisons Cre-lox dans la souris et de la puissance de l'imagerie multicouleur... ce papier n'est juste que la validation d'une technique qui pourrait (pour ceux qui en auront la patience et les moyens!!) avoir de nombreuses applications.
Transgenic strategies for combinatorial expression of fluorescent
proteins in the nervous system pp56 - 62
A combination of genetic tricks and fancy fluorescent proteins is used
to develop the Technicolor version of Golgi staining, 'Brainbow', in
which hundreds of individual neurons are painted, each with a
distinctive hue. This technology should not only boost mapping efforts
in normal or diseased brains, but could also be applied to other
complex cell populations, such as the immune system.
Oui rien que pour les photos ca vaut le coup!! Très beau papier en effet...
V.
Aller un autre pour le plaisir... toujours chez Nature:
Characterizing the cancer genome in lung adenocarcinoma.
Nature advance online publication 4 November 2007 | doi:10.1038/nature06358; Received 12 April 2007; Accepted 10 October 2007; Published online 4 November 2007
Somatic alterations in cellular DNA underlie almost all human
cancers1. The prospect of targeted therapies2 and the development
of high-resolution, genome-wide approaches3–8 are now spurring
systematic efforts to characterize cancer genomes. Here we report
a large-scale project to characterize copy-number alterations in
primary lung adenocarcinomas. By analysis of a large collection
of tumours (n5371) using dense single nucleotide polymorphism
arrays, we identify a total of 57 significantly recurrent events. We
find that 26 of 39 autosomal chromosome arms show consistent
large-scale copy-number gain or loss, of which only a handful have
been linked to a specific gene. We also identify 31 recurrent focal
events, including 24 amplifications and 7 homozygous deletions.
Only six of these focal events are currently associated with known
mutations in lung carcinomas. The most common event, amplification
of chromosome 14q13.3, is found in 12% of samples.
On the basis of genomic and functional analyses, we identify
NKX2-1 (NK2 homeobox 1, also called TITF1), which lies in the
minimal 14q13.3 amplification interval and encodes a lineagespecific
transcription factor, as a novel candidate proto-oncogene
involved in a significant fraction of lung adenocarcinomas. More
generally, our results indicate that many of the genes that are
involved in lung adenocarcinoma remain to be discovered.
http://www.nature.com/nature/journal...ture06358.htmlhttp://www.nature.com/nature/journal...ture06358.html
V.
C'est quand même pas mal Nature cette semaine......
Identification of Tim4 as a phosphatidylserine receptor.
Masanori Miyanishi1,2, Kazutoshi Tada2{, Masato Koike3, Yasuo Uchiyama3, Toshio Kitamura4 & Shigekazu Nagata1,2,5
In programmed cell death, a large number of cells undergo apoptosis,
and are engulfed by macrophages to avoid the release of
noxious materials from the dying cells1,2. In definitive erythropoiesis,
nuclei are expelled from erythroid precursor cells and
are engulfed by macrophages. Phosphatidylserine is exposed on
the surface of apoptotic cells3 and on the nuclei expelled from
erythroid precursor cells4; it works as an ‘eat me’ signal for phagocytes5,6.
Phosphatidylserine is also expressed on the surface of
exosomes involved in intercellular signalling7. Here we established
a library of hamster monoclonal antibodies against mouse peritoneal
macrophages, and found an antibody that strongly inhibited
the phosphatidylserine-dependent engulfment of apoptotic
cells. The antigen recognized by the antibody was identified by
expression cloning as a type I transmembrane protein called Tim4
(T-cell immunoglobulin- and mucin-domain-containing molecule;
also known as Timd4)8. Tim4 was expressed in Mac11 cells
in various mouse tissues, including spleen, lymph nodes and fetal
liver. Tim4 bound apoptotic cells by recognizing phosphatidylserine
via its immunoglobulin domain. The expression of Tim4 in
fibroblasts enhanced their ability to engulf apoptotic cells. When
the anti-Tim4 monoclonal antibody was administered into mice,
the engulfment of apoptotic cells by thymic macrophages was
significantly blocked, and the mice developed autoantibodies.
Among the other Tim family members, Tim1, but neither Tim2
nor Tim3, specifically bound phosphatidylserine. Tim1- or Tim4-
expressing Ba/F3 B cells were bound by exosomes via phosphatidylserine,
and exosomes stimulated the interaction between Tim1
and Tim4. These results indicate that Tim4 and Tim1 are phosphatidylserine
receptors for the engulfment of apoptotic cells, and
may also be involved in intercellular signalling in which exosomes
are involved.
http://www.nature.com/nature/journal...ture06307.htmlhttp://www.nature.com/nature/journal...ture06307.html
V.
Salut,
Voilà un truc sympa :
A single positively selected West Nile viral mutation confers increased virogenesis in American Crows
Brault AC, Huang CY, Langevin SA, Kinney RM, Bowen RA, Ramey WN, Panella NA, Holmes EC, Powers AM, Miller BR.
Center for Vector-Borne Diseases and Department of Pathology, Microbiology and Immunology, School of Veterinary Medicine, University of California, Davis, California 95616, USA.
West Nile virus (WNV), first recognized in North America in 1999, has been responsible for the largest arboviral epiornitic and epidemic of human encephalitis in recorded history. Despite the well-described epidemiological patterns of WNV in North America, the basis for the emergence of WNV-associated avian pathology, particularly in the American crow (AMCR) sentinel species, and the large scale of the North American epidemic and epiornitic is uncertain. We report here that the introduction of a T249P amino acid substitution in the NS3 helicase (found in North American WNV) in a low-virulence strain was sufficient to generate a phenotype highly virulent to AMCRs. Furthermore, comparative sequence analyses of full-length WNV genomes demonstrated that the same site (NS3-249) was subject to adaptive evolution. These phenotypic and evolutionary results provide compelling evidence for the positive selection of a mutation encoding increased viremia potential and virulence in the AMCR sentinel bird species.
Nat Genet. 2007 Sep;39(9):1162-6. Epub 2007 Aug 12
Cordialement,
Pas mal, pas malEn accès libre sur PubMed
(A)symmetric stem cell replication and cancer.
Dingli D, Traulsen A, Michor F.
Program for Evolutionary Dynamics, Harvard University, Cambridge, Massachusetts, United States of America.
Most tissues in metazoans undergo continuous turnover due to cell death or epithelial shedding. Since cellular replication is associated with an inherent risk of mutagenesis, tissues are maintained by a small group of stem cells (SCs) that replicate slowly to maintain their own population and that give rise to differentiated cells. There is increasing evidence that many tumors are also maintained by a small population of cancer stem cells that may arise by mutations from normal SCs. SC replication can be either symmetric or asymmetric. The former can lead to expansion of the SC pool. We describe a simple model to evaluate the impact of (a)symmetric SC replication on the expansion of mutant SCs and to show that mutations that increase the probability of asymmetric replication can lead to rapid mutant SC expansion in the absence of a selective fitness advantage. Mutations in several genes can lead to this process and may be at the root of the carcinogenic process.
PLoS Comput Biol. 2007 Mar 16;3(3):e53. Epub 2007 Feb 1.
Je ne sais pas dans quel journal c'est publié... Z'avez entendu parlé des deux équipes qui ont réussit a réversé des cellules de peau en cellules souches ?
Bonjour,
pour ceux qui ont un peu de temps à perdre je conseille la video proposée en supplementary material de l'article du Nature de cette semaine consacré à l'étude du (mega !)-complexe protéique qui forme le pore nucléaire des eucaryotes (dans cet article, il s'agit évidemment du pore nucleaire de la levure).
---------------------------------
Article
Nature 450, 695-701 (29 November 2007) | doi:10.1038/nature06405; Received 20 April 2007; Accepted 22 October 2007
The molecular architecture of the nuclear pore complex
Frank Alber1,4, Svetlana Dokudovskaya2,4,5, Liesbeth M. Veenhoff2,4,5, Wenzhu Zhang3, Julia Kipper2,5, Damien Devos1,5, Adisetyantari Suprapto2,5, Orit Karni-Schmidt2,5, Rosemary Williams2, Brian T. Chait3, Andrej Sali1 & Michael P. Rout2
Nuclear pore complexes (NPCs) are proteinaceous assemblies of approximately 50 MDa that selectively transport cargoes across the nuclear envelope. To determine the molecular architecture of the yeast NPC, we collected a diverse set of biophysical and proteomic data, and developed a method for using these data to localize the NPC's 456 constituent proteins (see the accompanying paper). Our structure reveals that half of the NPC is made up of a core scaffold, which is structurally analogous to vesicle-coating complexes. This scaffold forms an interlaced network that coats the entire curved surface of the nuclear envelope membrane within which the NPC is embedded. The selective barrier for transport is formed by large numbers of proteins with disordered regions that line the inner face of the scaffold. The NPC consists of only a few structural modules that resemble each other in terms of the configuration of their homologous constituents, the most striking of these being a 16-fold repetition of 'columns'. These findings provide clues to the evolutionary origins of the NPC.
-----------------------------------------------
Pour la vidéo :
http://www.nature.com/nature/journal...ture06405.html
